Protein C deficiency in splanchnic venous thrombosis |
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| Authors: | D Green D R Ganger A T Blei |
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| Affiliation: | 1. Atherosclerosis Program, Rehabilitation Institute, Chicago, Illinois, USA;2. the Gastroenterology Section, Department of Medicine, Northwestern University Medical School, Chicago, Illinois, USA;1. School of Semiconductor Science and Technology, South China Normal University, Guangzhou 510631, China;2. Guangdong Provincial Key Laboratory of Chip and Integration Technology, Guangzhou 510631, China;3. Institute of Semiconductors, Guangdong Academy of Sciences, Guangzhou 510650, China;4. School of Optoelectronic Science and Engineering, University of Electronic Science and Technology of China, Chengdu 610054, China;5. State Key Laboratory of Bioelectronics, School of Biological Sciences & Medical Engineering, Southeast University, Nanjing 210096, China;1. Department of Respiratory Medicine, Hospital del Mar – IMIM, DCEXS, Pompeu Fabra University, Barcelona, Spain;2. Department of Pharmacy, Hospital del Mar, Barcelona, Spain |
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| Abstract: | Deficiencies of protein C activity and antigen were observed in eight consecutive patients with splanchnic venous thrombosis. There was a significant reduction in the ratio of protein C to factor X. Six of the eight patients had a decrease in antithrombin III, but free protein S antigen was within normal limits in all but two subjects. It is proposed that a thrombogenic stimulus such as stasis, altered hormonal milieu, or failure of hepatic clearance of activated coagulants results in consumption of protein C and antithrombin III, predisposing to splanchnic venous occlusion. This further impairs hepatic function, prevents restitution of protein C and antithrombin levels, and promotes continuing venous thrombosis. Thus, a vicious cycle of thrombosis and hepatic damage is perpetuated. |
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